Induction of Undifferentiated Tumors by Jc Virus in the Cerebrum of Rats

Ohsumi, Shozo; Motoi, Makoto; Ogawa, Katsuo

doi:10.1111/j.1440-1827.1986.tb03116.x

Cited by 24 publications

(13 citation statements)

References 6 publications

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“…The family is named for some members’ ability to induce various types of tumors in experimentally infected animals. For example, the polyomaviruses BKV and JCV, which persistently infect the urinary epithelia in a great majority of humans, can cause tumors in experimentally inoculated rodents (Corallini et al, 1978; Ohsumi et al, 1986). Although BKV and JCV have been indirectly associated with the development of various forms of human cancer, such as prostate cancer and colorectal cancer (respectively), conclusive proof of a causal relationship between BKV or JCV and human cancers has remained elusive (reviewed in (Abend et al, 2009; Maginnis and Atwood, 2009)).…”

Section: Introductionmentioning

confidence: 99%

Merkel Cell Polyomavirus and Two Previously Unknown Polyomaviruses Are Chronically Shed from Human Skin

Schowalter

Pastrana

Pumphrey

et al. 2010

Cell Host & Microbe

512

595

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Summary Mounting evidence supports the concept that Merkel cell polyomavirus (MCV) is a causal factor underlying most cases of a highly lethal form of skin cancer known as Merkel cell carcinoma. To explore the possibility that polyomaviruses commonly infect healthy human skin, we developed an improved rolling circle amplification (RCA) technique to isolate circular DNA viral genomes from skin swab specimens. Complete MCV genomes were recovered from 14/35 (40%) healthy adults, providing the first full-length, apparently wild-type cloned genomes for this polyomavirus species. RCA analysis also revealed the existence of two previously unknown polyomavirus species that we name human polyomavirus-6 (HPyV6) and HPyV7. Biochemical experiments show that polyomavirus DNA is shed from the skin in the form of assembled virions. A pilot serological study indicates that infection or co-infection with the three skin-tropic polyomaviruses is very common. Thus, at least three polyomavirus species are constituents of the human skin microbiome.

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Section: Introductionmentioning

confidence: 99%

Merkel Cell Polyomavirus and Two Previously Unknown Polyomaviruses Are Chronically Shed from Human Skin

Schowalter

Pastrana

Pumphrey

et al. 2010

Cell Host & Microbe

512

595

View full text Add to dashboard Cite

show abstract

“…JCV can induce tumor formation in small rodents including hamsters [92–96] and rats [97], and in non-human primates including owl monkeys and squirrel monkeys [98–105] (Table 1). The tumor type, origin, and characteristics vary between host species and also depend on the route of inoculation and strain of virus utilized.…”

Section: Jcv and Tumorigenesis In Animal Modelsmentioning

confidence: 99%

“…The rats show signs of neurological illness beginning at 21 weeks post-inoculation such as weakness, ataxia, and death. Also, JCV-induced tumors are oncogenic when transplanted into new experimental rats [97]. While there is a strong correlation of JCV-induced tumors in rats, there are few reports that have followed this study.…”

Section: Jcv and Tumorigenesis In Animal Modelsmentioning

confidence: 99%

JC Virus: An oncogenic virus in animals and humans?

Maginnis

Atwood

2009

Seminars in Cancer Biology

106

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JCV is a human polyomavirus of the Polyomaviridae family, which also includes BK virus and simian vacuolating virus 40 (SV40). JC virus (JCV) was first isolated in 1971 from the brain of a patient with Progressive Multifocal Leukoencephalopathy (PML). Like other polyomaviruses, JCV has a restricted host range. The virus infects the majority of the human population with seroconversion occurring during adolescence. JCV has a limited and specific tissue tropism infecting the kidney and oligodendrocytes and astrocytes in the central nervous system (CNS). Initial JCV infection is generally asymptomatic in immunocompetent hosts, and it establishes a persistent infection in the kidney and possibly bone marrow. In immunocompromised individuals JCV can cause a lytic infection in the CNS and lead to development of the fatal, demyelinating disease PML. The name polyoma is derived from the Greek terms: poly, meaning many, and oma, meaning tumors, owing to the capacity of this group of viruses to cause tumors. JCV inoculation of small animal models and non-human primates, which are not permissive to a productive JCV infection, leads to tumor formation. Given the ubiquitous nature of the virus and its strong association with cancer in animal models, it is hypothesized that JCV plays a role in human cancers. However, the role for JCV in human cancers and tumor formation is not clear. Some researchers have reported an association of JCV with human cancers including brain tumors, colorectal cancers, and cancers of the gastrointestinal tract, while other groups report no correlation. Here, we review the role of JCV in cancers in animal models and present the findings on JCV in human cancers.

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“…The oncogenic potential of JCV was discovered when the virus was injected into the brain of Syrian hamsters inducing aneuploid tumors (Walker et al, 1973; Reiss and Khalili, 2003). In a broad range of experiments with several animal models, the oncogenic potential of JCV has been further established (London et al, 1978; Ohsumi et al, 1986). Transgenic mice that express JCV T‐antigen (T‐Ag) can develop tumors of the pituitary gland and malignant peripheral nerve sheath tumors that resemble rare neoplasms that can occur in patients with neurofibromatosis (Gordon et al, 2000; Shollar et al, 2004).…”

Section: Oncogenic Viral and Bacterial Pathogensmentioning

confidence: 99%

The role of viral and bacterial pathogens in gastrointestinal cancer

Selgrad

Malfertheiner

Fini

et al. 2008

Journal Cellular Physiology

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The association of Helicobacter pylori (H. pylori) with gastric cancer is thus far the best understood model to comprehend the causal relationship between a microbial pathogen and cancer in the human gastrointestinal tract. Besides H. pylori, a variety of other pathogens are now being recognized as potential carcinogens in different settings of human cancer. In this context, viral causes of human cancers are central to the issue since these account for 10–20% of cancers worldwide. In the case of H. pylori and gastric cancer, as well as the human papillomavirus and anal cancer, the causal relationship between the infectious agent and the related cancer in the gastrointestinal tract has been clearly confirmed by epidemiological and experimental studies. Similarly, Epstein–Barr virus and the oncogenic JC virus are being suggested as possible causative agents for cancers in the upper and lower gastrointestinal tract. This review discusses various viral and microbial pathogens and their oncogenic properties in the evolution of gastrointestinal carcinogenesis and summarizes the available experimental data make a convincing agreement favoring the associations between infectious agents and specific human cancers.

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Induction of Undifferentiated Tumors by Jc Virus in the Cerebrum of Rats

Cited by 24 publications

References 6 publications

Merkel Cell Polyomavirus and Two Previously Unknown Polyomaviruses Are Chronically Shed from Human Skin

Merkel Cell Polyomavirus and Two Previously Unknown Polyomaviruses Are Chronically Shed from Human Skin

JC Virus: An oncogenic virus in animals and humans?

The role of viral and bacterial pathogens in gastrointestinal cancer

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